Bezold-Jarisch Reflex-Induced Cardiac Arrest During Colonoscopy Under Sedation: A Case Report

Introduction

The Bezold-Jarisch reflex (BJR) is a cardioinhibitory reflex characterized by predominant cardiac suppression, wherein stimulation of unmyelinated vagal afferent receptors in the left ventricle (either pharmacologically or through mechanical stretch) triggers signals that travel via the vagus nerve to the nucleus tractus solitarius in the brainstem [1,2]. Following central integration, these signals are relayed to the vasomotor center, resulting in enhanced vagal efferent activity that manifests as severe bradycardia, peripheral vasodilation, systemic hypotension, and, potentially, cardiac arrest [3,4]. As a normal physiological reflex, it primarily functions to slow the heart rate during hypovolemia, thereby prolonging diastole and increasing coronary blood flow [5]. It is a rare event that occurs during anesthesia. Nevertheless, factors related to anesthesia or surgical trauma can trigger the reflex, which can be difficult to diagnose because of its rarity [6]. When BJR occurs under anesthesia, it is often mistaken for an intraoperative circulatory adverse event [7]. Here, we describe what appears to the first successful resuscitation of a patient who experienced BJR-induced cardiac arrest while under sedation for outpatient colonoscopy. This case report is clinically significant as it raises awareness among anesthesiologists to consider the BJR as a potential yet often overlooked cause when managing patients with unexplained cardiovascular complications during general anesthesia, thereby enabling timely and appropriate clinical interventions.

Case Report

A 54-year-old man with weight of 75 kg and height of 162 cm (body mass index, 28.6 kg/m2) came to our outpatient clinic for gastroenteroscopy. He denied a history of cardiovascular disease but reported having lost consciousness 6 or 7 times while urinating over the last 20 years. Each episode of micturition syncope lasted 1–2 minutes, after which he would spontaneously regain consciousness. After these episodes, he would feel transient fatigue without other discomfort. Repeated electrocardiographic and cardiac ultrasound examinations at other hospitals failed to detect anything unusual. Two days before his visit to our outpatient clinic, he was examined at our hospital, where his electrocardiographic findings were unremarkable and his status was determined to be I on the New York Heart Association scale and II on the American Society of Anesthesiologists scale.

In our outpatient clinic, the patient had a heart rate of 66 bpm, blood pressure of 132/78 mmHg and peripheral oxygen saturation (SpO2) of 100%. The patient underwent sedation using butorphanol (0.2 mg), propofol (150 mg), and lidocaine (30 mg), then gastroscopy was performed. Propofol (30 mg) was administered intravenously before colonoscopy. When the colonoscope reached the rectosigmoid junction, the heart rate dropped sharply from 65 to 44 bpm, and the colonoscope was immediately withdrawn. Atropine (0.5 mg) was administered intravenously, and the heart rate rose to 51 bpm. The colonoscope was re-inserted and when it approached the rectosigmoid junction again, the heart rate dropped sharply to 45 bpm. The colonoscope was withdrawn again, atropine (0.5 mg) was administered, and the heart rate returned to 60 bpm.

On the third colonoscopy attempt, the heart rate suddenly dropped to 28 bpm, and cardiac arrest occurred. The patient was immediately given chest compressions, during which he received atropine (0.5 mg) and epinephrine (1 mg). Sinus rhythm recovered within 2 min, whereupon chest compressions were stopped. At this point, the patient had a heart rate of 160 bpm, blood pressure of 164/120 mmHg, and SpO2 of 96%. Within 3 min, heart rate decreased rapidly to 88 bpm, blood pressure to 69/42 mmHg and SpO2 to 91%. The patient awoke at this time and said he felt generalized weakness. To counteract the fluctuations in blood pressure, norepinephrine had to be delivered in 2 intravenous injections of 10 μg each before blood pressure stabilized at 101/62 mmHg within a few minutes after the second injection. The patient reported no other discomfort during this period. Bedside electrocardiography indicated sinus rhythm and ST segment depression of 0.05–0.1 mV at leads II, III, aVF, and V4–V6.

The patient had a history of syncope but had not undergone detailed systematic examinations to determine the underlying cause. Organic pathologies, such as cardiovascular or cerebrovascular diseases, could not be ruled out. Therefore, after successful resuscitation, a comprehensive diagnostic workup was required to identify the etiology and exclude other primary conditions that may have led to cardiac arrest. Consequently, the patient was referred to a syncope specialist team for further evaluation. At 20–60 min after cardiac arrest, routine blood tests showed normal cell counts as well as normal levels of glucose, electrolytes, cardiac enzymes, brain natriuretic peptide, and thyroid hormones. Transthoracic cardiac ultrasonography revealed slightly reduced amplitude of septal beating, left ventricular systolic function at the lower limit of normal, and ejection fraction of 52%. At 24 h after cardiac arrest, coronary angiography indicated no stenosis; findings were normal for carotid and abdominal ultrasonography, computed tomography of the chest and cervical spine, and cranial magnetic resonance imaging; and ambulatory electrocardiography indicated sinus rhythm, occasionally premature atrial beats, ST-T changes, and normal variability in the heart rate. Therefore, the cardiac arrest was considered to be caused by BJR. The patient was discharged on day 5 after cardiac arrest, and at telephone follow-up 4 months later, he indicated no syncope had occurred.

Discussion

BJR is usually diagnosed based on clinical manifestations after exclusion of organic pathology [6]. Our patient showed no evidence of organic pathology upon post-resuscitation examination. The clinical presentation – initial recurrent bradycardia with hypotension progressing to syncope or cardiac arrest – was more consistent with BJR rather than typical vasovagal syncope [8,9]. Notably, vasovagal reactions characteristically manifest with initial tachycardia and hypotension as primary symptoms [10]. During the painless endoscopic examination, prolonged preoperative fasting likely induced hypovolemia, while subsequent anesthesia further exacerbated vascular dilation, potentially creating a significant volume-depleted state [11]. This hemodynamic alteration triggered compensatory hypercontractility of the myocardium, resulting in abnormal stimulation of ventricular mechanoreceptors and subsequent BJR activation [8]. Furthermore, the potential light anesthesia plane during the procedure may have inadequately blocked nociceptive signaling. Endoscopic manipulation consequently provoked catecholamine release and other biochemical mediators that additionally contributed to BJR initiation through chemoreceptor stimulation [12]. However, prior to undergoing painless gastroenteroscopy, the anesthesiologist should have conducted more thorough examinations and evaluations to determine whether the patient had any underlying organic pathology, clarify the diagnosis, and implement targeted preventive measures and treatment. This is the key lesson we can draw from this case.

A previously reported cause of perioperative BJR is a sudden decrease in return blood volume due to a change in the patient’s body position from a supine position to a beach chair, semi-sitting, or right lateral recumbent folding-knife position [13]. Normal cardiac rhythm can be restored by returning the patient to the supine position or administering atropine [14]. Another reported cause is intrathecal anesthesia, which can induce BJR due to peripheral vasodilatation and insufficient blood volume from preoperative fasting [15]. A patient experienced recurrent cardiac arrest suspected of being due to BJR while under sciatic nerve block and general anesthesia, and was resuscitated through chest compression, antihypertensive medications, and coronary stent placement [16]. Administration of dobutamine, isoproterenol, and other β-receptor agonists may increase the risk of perioperative BJR [17,18]. Clinicians should be aware of the danger of failing to diagnose BJR correctly when it occurs under anesthesia, which can delay effective treatment [19].

Our review of the literature suggests several steps that clinicians can take to prevent perioperative BJR and to recognize and treat it if it occurs. Firstly, for patients with a history of unexplained syncope, clinicians should maintain a high index of suspicion for potential BJR etiology and implement appropriate preparatory measures. Before anesthesia, blood volume should be supplemented [12]. Inadequate depth of anesthesia can cause the body to perceive painful stimuli and release chemicals such as catecholamines, which can induce BJR, so maintaining an appropriate depth of anesthesia is necessary [20]. The position should be adjusted slowly during the operation; in case of cardiac arrest, the heart may resume beating automatically after returning to the lying position [12]. In the event of bradycardia and hypotension thought to be due to BJR, administering ephedrine may be more effective than administering atropine; if cardiac arrest occurs, prompt administration of epinephrine together with chest compressions is usually successful [21]. Preoperative infusion of the 5-HT3 receptor antagonist ondansetron can reduce the risk of BJR, but its role still needs to be further verified [22]. Preoperative injection of the β-receptor blockers propranolol or metoprolol can also reduce risk of BJR, but such drugs can also decrease cardiac output, which may aggravate perioperative hypotension [23].

Conclusions

To the best of our knowledge, this is the first reported case of BJR during colonoscopy under sedation, and we review the literature on causes, treatment, and prevention of perioperative BJR. Adequate assessment of patients before anesthesia and prompt resuscitation are essential for minimizing the risk of BJR and serious complications if it occurs.